被撤回的出版物: MicroRNA-379 acts as a tumor suppressor in non-small cell lung cancer by targeting the IGF-1R-mediated AKT and ERK pathways (Retracted article. See vol. 48, 2022)

Lung cancer is one of the most common types of malignancy in humans and is a leading cause of cancer-related deaths among men and women worldwide. Aberrantly expressed microRNAs in non-small cell lung cancer (NSCLC) contribute to tumor occurrence and development as either tumor suppressors or promoters. MicroRNA-379 (miR-379) is dysregulated in several types of human cancer. However, its expression pattern, role and underlying mechanism in NSCLC progression and metastasis are poorly understood. In this study, assay of reverse transcription-quantitative polymerase chain reaction showed that miR-379 was downregulated in both NSCLC tissue and cell lines. Low miR-379 expression in NSCLC tissues was significantly correlated with TNM stage and lymph node metastasis. In addition, functional experiments revealed that restoring the expression of miR-379 inhibited cell proliferation, migration and invasion of NSCLC. The insulin-like growth factor receptor-1 (IGF-1R) was identified as a direct target of miR-379 in NSCLC. IGF-1R was highly expressed in NSCLC tissues and inversely correlated with miR-379 expression. Downregulation of IGF-1R had tumor suppressive roles similar to that of miR-379 overexpression on NSCLC cell proliferation, migration and invasion. Moreover, the upregulation of IGF-1R effectively rescued the tumor suppressive roles induced by miR-379 overexpression in NSCLC. The resumption of the expression of miR-379 inhibited the activation of AKT and ERK signaling pathways in NSCLC. These findings suggested that miR-379 acts as a tumor suppressor in NSCLC by directly targeting IGF-1R and indirectly regulating AKT and ERK signaling pathways. miR-379 provides novel therapeutic targets for the treatment of patients with this disease.